Addition/Correction pubs.acs.org/biochemistry
Correction to Molecular Basis for Fe(III)-Independent Curcumin Potentiation of Cystic Fibrosis Transmembrane Conductance Regulator Activity Guangyu Wang* Biochemistry 2015, 54 (18), 2828−2840. DOI: 10.1021/acs.biochem.5b00219 The correct version of Figure 8 appears here. Line 6 of page 2835, “from 0.164 to 0.180” is corrected as “from 0.333 to 0.396”. Line 9 of page 2835, “from 0.180 to 0.001” is corrected as “from 0.396 to 0.016”.
Figure 8. Effects of spontaneous disulfide cross-linking of K162C to S795C on single-channel opening. (A) Representative inside-out single-channel currents of S795C/K162C/V510A across an excised HEK-293T micropatch. The holding potential was −60 mV. The channel was activated with 1.5 mM MgATP and 24 units/mL PKA, followed by PKI. Diamide was used to induce formation of a disulfide bond, while DTT was employed to disrupt the disulfide bond. (B) Changes in the open probability of S795C/K162C/V510A (n = 3; *P < 0.001, from an unpaired Student’s t test). Inside-out macroscopic currents of (C) K162C/V510A and (D) S795C/V510A across an excised HEK-293T patch. The channel was activated with 1.5 mM MgATP and 24 units/mL PKA, followed by PKI (1.4 μg/mL). CFTRinh172 (5−10 μM) or glibenclamide (200 μM) was used to block the total CFTR-mediated current. (E) Relative changes in currents in response to diamide (10−20 μM) and DTT (5−10 mM) (n = 3; *P < 0.001, from an unpaired Student’s t test). Received: May 26, 2015 Published: June 23, 2015 © 2015 American Chemical Society
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DOI: 10.1021/acs.biochem.5b00570 Biochemistry 2015, 54, 4161−4161
